The effect of prenatal stressor exposure on child cognitive functioning: the importance of timing of stress and domain of cognition.

Prenatal stress has been associated with poor cognitive outcomes in offspring, but the evidence about the role of exact timing of exposure is mixed and that about causal mechanisms is limited. Using the Avon Longitudinal Study of Parents and Children, this study (N = 4,525) explored the role of inflammation in the association between timing of prenatal-stressor exposure and cognitive functioning in middle childhood (ages 9-11 years). Prenatal-stressor exposure was measured at two timepoints (until 18 weeks gestation and from then until 8 weeks postpartum). Cognitive outcomes included working memory, spelling, reading (speed, accuracy, comprehension), response inhibition, selective attention, attentional control, social cognition, and verbal ability. Path models examined mediation via inflammatory markers (IL-6 and CRP, at age 9 years), and factor analysis on the outcomes identified broad cognitive domains. The findings from regression models controlling for confounders and mutually adjusting for early and later prenatal-stressor exposure suggest that early prenatal events impacted only reading comprehension. Later-prenatal events had a detrimental effect on response inhibition, social cognition, and verbal ability, but a seemingly beneficial effect on reading accuracy and comprehension, likely due to suppression. Early prenatal events had no impact on the broad domains identified by factor analysis (reading/spelling, attention, and social communication), but later-prenatal events were inversely associated with both reading/spelling and social communication. Inflammation did not mediate prenatal-stressor effects on either broad domains or specific outcomes. It appears that stressor exposure later rather than early in gestation impacted children's reading/spelling and social communication. There was no evidence that inflammation mediated that impact.